Anderson et al. found that Gal-9 and its receptor TIM-3 contribute to inflammation by increasing proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) expression from MNs and dendritic cells, whereas Arikawa et al. found that Gal-9 suppresses murine arthritis and TNF-α secretion [23, 24]. The gene discussed is HAVCR2; the disease is arthritic joint disease.